IL1B and Alzheimer disease: Of note, most studies regarding the role of Lcn2 in CNS disease/injury until now were performed in acute models of CNS injury (which may cause stronger, short-term, induction of Lcn2), in contrast to the chronic transgenic AD model studied here (in which—in comparison to models of acute injury—Lcn2 expression may be less strong, which may also be the case for the expression of other inflammatory mediators such as interleukin 1 beta (IL-1β, also see, Additional file 1: Figure S9)).